000162227 001__ 162227
000162227 005__ 20251113150202.0
000162227 0247_ $$2doi$$a10.1186/s12864-025-11725-4
000162227 0248_ $$2sideral$$a144758
000162227 037__ $$aART-2025-144758
000162227 041__ $$aeng
000162227 100__ $$0(orcid)0000-0003-2436-7205$$aMoreno-García, Leticia
000162227 245__ $$aCircular RNA expression in ALS is progressively deregulated and tissue-dependent
000162227 260__ $$c2025
000162227 5060_ $$aAccess copy available to the general public$$fUnrestricted
000162227 5203_ $$aBackground
There is increasing evidence on the role of circular RNAs (circRNAs) in neuronal and muscular processes. Accordingly, their dysregulation is associated with neurodegenerative diseases and myopathies. We investigated circRNA expression in the central nervous system (CNS) and skeletal muscle, the two main tissues affected in amyotrophic lateral sclerosis (ALS).
Results
Based on circRNA sequencing analysis in spinal cord from ALS mice (SOD1G93A) followed by a literature search, 30 circRNAs potentially involved in ALS were tested. All selected circRNAs were downregulated in the SOD1G93A spinal cord, whereas only half of these were quantifiable and were generally upregulated in quadriceps muscle of SOD1G93A mice. Such tissue-dependent expression pattern was observed in both sexes and circRNA abundance in the spinal cord was higher than in the muscle, both in wild type and in SOD1G93A mice. Finally, we assessed the 18 circRNAs with the largest expression differences and the highest degree of interspecies conservation in brain samples from sporadic ALS (sALS) patients and healthy controls. Similar to the mouse model, circRNA levels tended to decrease in the CNS of sALS patients.
Conclusions
Expression of circRNAs may be systematically altered in the two tissues most affected by ALS in a progressive and opposed manner. Although more detailed studies are warranted, circRNAs are potentially related to ALS etiopathogenesis and could possibly serve as future biomarkers, therapeutic targets, or customized therapeutic tools to modulate the pathology.
000162227 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII/CB18-05-0037$$9info:eu-repo/grantAgreement/ES/ISCIII/FEDER/PI21-00372$$9info:eu-repo/grantAgreement/ES/MICINN-AEI/PRTR-C17.I1$$9info:eu-repo/grantAgreement/ES/UZ/2018-BIO-03
000162227 540__ $$9info:eu-repo/semantics/openAccess$$aby-nc-nd$$uhttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
000162227 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000162227 700__ $$0(orcid)0000-0002-7277-4318$$aMoreno-Martínez, Laura$$uUniversidad de Zaragoza
000162227 700__ $$0(orcid)0000-0002-7955-7164$$ade la Torre, Miriam
000162227 700__ $$aMacías-Redondo, Sofía
000162227 700__ $$0(orcid)0000-0001-7646-386X$$aGarcía-Redondo, Alberto
000162227 700__ $$0(orcid)0000-0001-5687-6704$$aOsta, Rosario$$uUniversidad de Zaragoza
000162227 700__ $$0(orcid)0000-0002-7243-1737$$aToivonen, Janne Markus$$uUniversidad de Zaragoza
000162227 700__ $$0(orcid)0000-0001-5193-7782$$aCalvo, Ana Cristina$$uUniversidad de Zaragoza
000162227 7102_ $$11001$$2420$$aUniversidad de Zaragoza$$bDpto. Anatom.,Embri.Genét.Ani.$$cÁrea Genética
000162227 7102_ $$11012$$2315$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Farmacología
000162227 773__ $$g26 (2025), 576 [21 pp.]$$pBMC genomics$$tBMC Genomics$$x1471-2164
000162227 8564_ $$s7767392$$uhttps://zaguan.unizar.es/record/162227/files/texto_completo.pdf$$yVersión publicada
000162227 8564_ $$s1789174$$uhttps://zaguan.unizar.es/record/162227/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000162227 909CO $$ooai:zaguan.unizar.es:162227$$particulos$$pdriver
000162227 951__ $$a2025-11-13-15:00:40
000162227 980__ $$aARTICLE